Effect of letrozole in carcinogen-plus-estrogen-induced endometrial hyperplasia in mice

PURPOSE: To evaluate the effects of letrozole (Ltz) in carcinogen+estrogen-induced endometrial hyperplasia. METHODS: BALB/c female mice were divided into four groups of 12 animals each receiving an intrauterine dose of N-ethyl-N-nitrosourea (ENU) and weekly subcutaneous injections of estradiol hexaidrobenzoate (EHB), except for group I(control). The groups were divided in I (control), II (ENU+EHB), III (ENU+EHB+MPA) and IV (ENU+EHB+Ltz). Group III also received intramuscular injections of MPA (medroxy progesterone acetate) every four weeks, while group IV received oral doses of Ltz daily. At the end of 16 weeks, the animals were sacrificed, and blood samples were collected for the measurement of serum estradiol and progesterone levels. Uterine histological sections were made to evaluate the presence of endometrial proliferative lesions. Differences between groups were evaluated with student's t test, ANOVA and chi-square test. RESULTS: Groups ENU+EHB, ENU+EHB+MPA and ENU+EHB+Ltz showed varying degrees of endometrial hyperplasia. The incidence of hyperplasia in groups ENU+EHB and ENU+EHB+Ltz was higher and more severe than in group ENU+EHB+MPA. Control group showed lower levels of serum estradiol than the other groups. CONCLUSION: There was no evidence that letrozole could act as an antiestrogenic drug in the development of endometrial proliferative lesions.

Conservative treatment for atypical endometrial hyperplasia: what is the most effective therapeutic method? / 부인종양

No abstract available.

[Immunohistochemical expression of estrogen and progesterone receptors in endometrial hyperplasia and endometrioid carcinoma]

Endometrial carcinoma [EC] is the most common gynecologic malignancy; however, mechanisms underlying its pathogenesis remain obscure. Endometrial carcinoma has been classified into two major categories: type I [related to estrogen or endometrioid adenocarcinoma] and type II [unrelated to estrogen]. Estrogen is the main trigger for the abnormal proliferation in the endometrial epithelium but progesterone can inhibit this process. The aim of this study was to analyze the expression of estrogen and progesterone receptors in all types of endometrial hyperplasia in comparison to endometrioid adenocarcinoma of endometrium. Forty-seven specimens including 23 cases of histopathologically confirmed hyperplastic endometrium [12 simple hyperplasia, 5 complex hyperplasia without atypia, and 6 complex hyperplasia with atypia] and 24 cases of endometrial carcinoma were studied. Immunohistochemical staining of estrogen and progesterone receptors was performed in paraffin-embedded blocks and expression of estrogen and progesterone receptors were scored according to the proportion of positive staining cells. Overexpression of progesterone receptors was seen in 18 [75%] out of 24 cases of endometrial carcinoma and 23 [100%] of all types of endometrial hyperplasia. The aforesaid differences were statistically significant [P=0.023]. 70.8% of cases with endometrial carcinoma were 3+ for immunohistochemical staining of progesterone receptors as were 85.7% of the cases with endometrial hyperplasia; the difference being also statistically significant [P=0.02]. Considering the increased proportion of progesterone receptor expression in all types of hyperplastic endometrium in comparison to endometrial carcinoma, hormonal therapy by progestinal agents is recommended as a treatment of choice

Hiperplasia endometrial atípica en pacientes infértiles: manejo conservador / Atypical endometrial hyperplasia in infertile patients: conservative management

Se presentan 4 pacientes infértiles portadoras de hiperplasia endometrial con atipías que se manejaron en forma conservadora en nuestro hospital. Tres pacientes recibieron acetato de medroxiprogesterona oral por 6 meses (100 mg día) con demostración histológica de regresión de la lesión e inducción de ovulación subsecuente. Un caso no recibió tratamiento por presentar regresión espontánea de su patología endometrial. Tres pacientes se embarazaron (dos únicos y un gemelar) obsteniéndose un aborto espontáneo y tres recién nacidos de término. Se concluye que el manejo conservador de la hiperplasia endometrial con atipías, empleando acetato de medroxiprogesterona oral en altas dosis, es efectivo. Una vez corregidos los ciclos anovulatorios con inductores de ovulación es posible obtener gestaciones viables

Perspectivas de manejo en la hiperplasia endometrial. Informe preliminar / The outlook for the management of endometrial hyperplasia. a preliminary report

Con el propósito de encontrar un tratamiento menos traumático y unificar criterios en nuestro medio en el menejo de la Hiperplasia Endometrial (HE) realizamos una prueba farmacológica en siete mujeres con HE y hemorragia uterina en edad fértil (n=3) y perimenopaútisicas (n=4). Se les prescribió noretindrona (NET) 5 mg/45d. No se observaron efectos colaterales indesables. Las siete pacientes mostraron regresión endometrial, dos de las tres jóvenes lograron embarazo a término y las cuatro perimenopaúsicas no volvieron a menstruar. En estas observaciones preliminares no hubo ningún fenómeno de asociación entre hormonas esteroides gonadales (Estradiol E-2, estrona E-1, Progesterona P-4) con la histología endometrial

Hiperplasia endometrial: diagnóstico, tratamiento y manejo clínico / Endometrial hyperplasia: diagnosis, treatment and clinical management

Se investigan 57 casos consecutivos de hiperplasia endometrial, y se analiza su reversibilidad con tratamiento médico. Fueron tratadas con acetato de medroxiprogesterona (habitulamente 10 a 15 mg/día durante 21 días al mes, durane un lapso mínimo de tres meses), salvo dos pacientes que se manejaron con citrato de clocmifeno. Las pacientes eran anovulantes crónicas (59,6%) o bien climatéricas (40,4%). La mayoria de las biopsias de endometrio (84%) se obtuvieron mediante cánulas intrauterinas con jeringa de aspiración. Se encontraron hiperplasias endometriales simples (29,8%, glanduloquísticas (29,8%), adenomatosas (35,1%) y atípicas (5,3%). Sólo dos casos no respondieron al tratamiento médico, requiriendo histerectomía. El tratamiento posterior se hizo consecuentemente con las diversas etiopatogenias encontradas. En todos los casos se aseguró la descamación endometrial periódica posterior. Se concluye proponiendo un protocolo combinado médico-quirurgico para el tratamiento y seguimiento de las pacientes con riesgo de hiperplasia endometrial